The invention relates to the surprising find that low density lipoprotein receptor-deficient mice (LDLr−/−) mice when fed with high energy diets produce controllable and consistent diabetic complications, especially renal damage, similar to the human pathophysiology and biological response. The invention thus comprises a method for discovering a preventive or therapeutic regimen for the prevention or treatment of diabetic micro- or macrovascular complications, comprising the steps of: a. feeding LDLr−/− mice, which have not been treated with streptozotocin, with a high energy diet; b. before, during and/or after this diet treating the mice with the preventive or therapeutic regimen; c. checking whether any change in the micro- or macrovascular system of the animal occurs. Specifically in such a method renal damage is assessed. Also use of said mice fed with a high energy diet for studying the diabetic micro- and macrovascular complications is part of the invention.

Provided are methods for identifying or monitoring a subject having, or at risk of developing, impaired glucose homeostasis. Carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF) is shown to be a biomarker for impaired glucose homeostasis and/or conditions characterized by β-cell dysfunction. Comparing a test level of CMPF in a subject to a control level identifies subjects having, or at risk of developing, impaired glucose homeostasis. Also provided are methods of causing impaired glucose homeostasis or β-cell dysfunction and methods of screening for compounds that affect the activity of β-cells. Also provided are methods for the treatment of β-cell dysfunction by reducing the physiological levels of CMPF in a subject as well as the use of a OAT modulator for the treatment of β-cell dysfunction.

Among the various aspects of the present disclosure is the provision of a method of detection, treatment, and monitoring of cardiovascular disease or a foot wound by detection of a novel biomarker, Fatty Acid Synthase (FAS). Briefly, therefore, the present disclosure is directed to methods that allow for improved, noninvasive, and reliable diagnosis of these conditions, particularly in subjects suffering from Type 2 Diabetes (T2D).

A prediction of type 2 diabetes development through quantitative analysis of N-glycans attached to the plasma proteins of a healthy person, which enables determination of whether the investigated person belongs to a risk group for type 2 diabetes development in the future. Using obtained quantitative percentages of all analyzed N-glycans as input variables of a model F: F(GP1, GP2, . . . , GPX; D, S), where X, D and S are parameters of the model F: X=total number of analyzed N-glycans; D=age of the investigated person; S=sex of the investigated person; male=1, female=0. Obtaining constants of the model F (GP1, GP2, . . . , GPX; D, S) by statistical data processing and modelling from analyzed population. Comparing obtained result F for the investigated person with a statistically determined threshold T, which defines the threshold of increased risk for type 2 diabetes (T2D) development in the future.

The present invention concerns a method for the in vitro detection of an increased risk of diabetic nephropathy in a subject suffering from diabetes and being normoalbuminuric. Another aspect of the invention pertains to a method for the in vitro identification of a marker for prediction of diabetic nephropathy. Finally, the invention concerns a kit comprising means for detecting at least two proteins selected from the group consisting of heparan sulfate proteoglycan core protein or fragments thereof, carbonic anhydrase 1, prothrombin or fragments thereof, tetranectin, CD59 glycoprotein, plasma serine protease inhibitor, mannan-binding lectin serine protease 2 or isoforms thereof, antithrombin-III, alpha-1-antitrypsin, collagen alpha-1(I) chain, alpha-enolase, histone H2B type 1-O, glutaminyl-peptide cyclotransferase, protein AMBP and zinc-alpha-2-glycoprotein.

The inventors have produced two high specificity and high affinity monoclonal antibodies that bind to human neuromedin U (NMU). Methods and compositions are provided for treating an individual in need thereof (e.g., an individual who is obese and/or has diabetes) by administering an anti-NMU/NMUR agent (e.g., an anti-NMU antibody). For example, methods and compositions are provided for increasing circulating insulin in an individual. Methods and compositions are also provided for detecting neuromedin U (NMU) (e.g., in a biological sample such as serum). Methods and compositions are also provided for predicting whether an individual will develop diabetes and/or PDAC, and for identifying an individual who would benefit from administration of an anti-NMU/NMUR agent.

The methods described herein enable the evaluation of compounds on subjects to assess their therapeutic efficacy or toxic effects. The target of analysis is the underlying biochemical process or processes (i.e., metabolic process) thought to be involved in disease pathogenesis. Molecular flux rates within the one or more biochemical processes serve as biomarkers and are quantitated and compared with the molecular flux rates (i.e., biomarker) from control subjects (i.e., subjects not exposed to the compounds). Any change in the biomarker in the subject relative to the biomarker in the control subject provides the necessary information to evaluate therapeutic efficacy of an administered drug or a toxic effect and to develop the compound further if desired.

The present invention relates to methods for diagnosing gestational diabetes mellitus (GDM) in a pregnant female.

A method of extracting organ metabolic functions using oral glucose tolerance tests (OGTTs) comprises: a step of measuring an amount of change over time in plasma glucose and plasma insulin at a regular time interval after a subject has consumed a certain quantity of a glucose solution; a step of extracting parameters associated with organ metabolism in a human body by applying the amount of change over time of the measured glucose and insulin to a human organ function model; and a step of diagnosing the metabolic function state of the subject using the extracted parameters.

Described herein are assays, methods, and devices for diagnosing/prognosing diabetes, metabolic syndrome, pre-diabetic state and/or the early-onset of diabetes in a subject. The assays, methods, and devices described herein can be configured to detect one or more long-coding RNAs in a sample from a subject.